Wang Z, Zhang G, Lin M
Department of Gynecology and Obstetrics, Xiehe Hospital, Tongji Medical University, Wuhan 430030.
J Tongji Med Univ. 1999;19(3):209-11. doi: 10.1007/BF02887736.
To explore the roles of mitochondria tRNA(leu)(UUR) gene mutation at nucleotide 3243 and the activity of cytochrome c oxidase in pathogenesis of preeclampsia, 57 patients with preeclampsia and 60 normotension pregnancy women were screened for tRNA(leu)(UUR) nt3243 A-->G mutation with the method of polymers chain reaction (PCR) and restriction fragment length polymorphism. Cytochrome c oxidase activity was determined by measuring the rate of cyanide-sensitive oxidation of reduced cytochrome c using luminosity photographer. The results showed that cytochrome c oxidase activity was significantly lower in the preeclampsia group (0.30 +/- 0.39/min, n = 32) than that in the controls (0.73 +/- 0.54/min, n = 26, P < 0.01). The mitochondria DNA mutation at position 3243 was not found in our series. The results suggested that the decreased activity of cytochrome c oxidase might impair the energy production, leading to the mitochondria dysfunction and placenta dysfunction in preeclampsia patients. Mitochondria dysfunction may be involved in the pathogenesis of preeclampsia. The mutation of mitochondria DNA may not be the common contributor of preeclampsia in our series.
为探讨线粒体tRNA(亮氨酸)(UUR)基因第3243位核苷酸突变及细胞色素c氧化酶活性在子痫前期发病机制中的作用,采用聚合酶链反应(PCR)和限制性片段长度多态性方法,对57例子痫前期患者和60例血压正常的孕妇进行tRNA(亮氨酸)(UUR) nt3243 A→G突变筛查。采用光度摄影法通过测定还原型细胞色素c的氰化物敏感氧化速率来确定细胞色素c氧化酶活性。结果显示,子痫前期组(0.30±0.39/min,n = 32)细胞色素c氧化酶活性显著低于对照组(0.73±0.54/min,n = 26,P<0.01)。在本研究系列中未发现第3243位的线粒体DNA突变。结果提示,细胞色素c氧化酶活性降低可能损害能量产生,导致子痫前期患者线粒体功能障碍和胎盘功能障碍。线粒体功能障碍可能参与子痫前期的发病机制。线粒体DNA突变可能不是本研究系列中子痫前期的常见病因。